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Test of Xq26.3–28 linkage in bipolar and unipolar affective disorder in families selected for absence of male to male transmission

Published online by Cambridge University Press:  02 January 2018

Ciaran Smyth ,
Gursharan Kalsi ,
Jon Brynjolfsson ,
Jane O'Neill ,
David Curtis ,
Larry Rifkin ,
Eamon Moloney ,
Patrice Murphy ,
Hannes Petursson  and
Hugh Gurling
Ciaran Smyth
Affiliation:
Molecular Psychiatry Laboratory, University College London Medical School
Gursharan Kalsi
Affiliation:
Molecular Psychiatry Laboratory, University College London Medical School
Jon Brynjolfsson
Affiliation:
Department of Psychiatry, University of Iceland
Jane O'Neill
Affiliation:
Molecular Psychiatry Laboratory, UCL Medical School
David Curtis
Affiliation:
Academic Department of Psychiatry, St Bartholomew's and Royal London School of Medicine and Dentistry, Whitechapel, London E1 1BB
Larry Rifkin
Affiliation:
Molecular Psychiatry Laboratory, UCL Medical School
Eamon Moloney
Affiliation:
Molecular Psychiatry Laboratory, UCL Medical School
Patrice Murphy
Affiliation:
Molecular Psychiatry Laboratory, UCL Medical School
Hannes Petursson
Affiliation:
Department of Psychiatry, Borgarspitalinn, Reýkjavik 108, Iceland
Hugh Gurling*
Affiliation:
Molecular Psychiatry Laboratory, UCL Medical School
*
Professor H. Gurling, Molecular Psychiatry Laboratory, University College London Medical School, Windeyer Building, 46 Cleveland Street, London WIP 6DB. Fax: 0171 436 5046; e-mail: [email protected]
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Abstract

Background

There have been several reports of linkage between genetic markers on the X chromosome at Xq26.3-28 and bipolar affective disorder in family samples obtained from distinct ethnic and geographical origins. As part of a genome search in a series of 23 UK and Icelandic families, specifically selected for their large size and power to resolve the issue of linkage heterogeneity, we have tested the hypothesis that there is a locus for a genetic subtype of bipolar affective disorder which is linked to this region.

Method

In families selected on the basis of absent male to male transmission for affective disorder, we performed two-point and FASTMAP multipoint linkage analyses with markers spanning the region between the genetic loci DXS102 and F8

Results

We found negative lod scores for several models of affection status in families selected under stringent and relaxed criteria for the absence of male to male transmission.

Conclusions

In the family sample we have obtained, our study provides no support for the presence of a locus increasing genetic susceptibility to bipolar affective disorder in this region of the X chromosome. It is likely that our finding reflects heterogeneity of linkage for bipolar and genetically related unipolar disorder that exists in specific ethnic populations. Alternatively the X-linked subtype of the disorder may have been present only in a few of our small families resulting in loss of power to detect the Xq26.3-28 linked subtype.

Type
Papers
Information
The British Journal of Psychiatry , Volume 171 , Issue 6 , December 1997 , pp. 578 - 581
Copyright
Copyright © 1997 The Royal College of Psychiatrists 

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